Hepatic retinol correlated negatively with sigma-dichlorodiphenyldichloroethane (sigma DDT) and and sigma-polybrominated diphenyl ethers (sigma PBDE) for all exposed animals. A negative correlation between kidney -tocopherol and sigma PCB concentrations was observed, whereas two positive significant correlations were observed between kidney retinol and sigma-chlordane-related compounds (sigma CHL) and dieldrin concentrations. Hepatic -tocopherol concentrations were significantly lower in exposed compared to controls, most likely due to a combination by OHC exposure and high dietary intake of unsaturated fatty acids. These results suggest that dietary exposure from OHC may, even

at low concentrations, possibly affect retinol and -tocopherol status in Arctic top predators.”
“2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent toxicant that alters normal brain learn more development and produces cognitive disability and motor dysfunction.

However, after decades of intense study, the molecular mechanisms of TCDD-induced neurotoxicity, the signaling pathways involved and its molecular targets in neurons still remain unknown. TCDD acts as an exogenous ligand LY3009104 mw of the aryl hydrocarbon receptor (AhR) that becomes a key signaling molecule in the regulation of the toxic and carcinogenic properties of TCDD. We have used NGF-differentiated pheochromocytoma (dPC12) cells to determine the type of cell death that takes place by TCDD toxicity. TCDD induced cell death in dPC12 cultures with an EC(50) of 218 +/- 24 nM, similar to that obtained in undifferentiated PC12 cells, 171 +/- 31 nM. Nuclear fragmentation was observed after TCDD incubation in parallel to an increase in caspase-3 activity. Staurosporine, which readily induced apoptosis in dPC12 cells, showed a similar increase in caspase-3 activity and the characteristic pattern of nuclear fragmentation. Flow cytometry measurements showed that dPC12 cells

in the presence see more of TCDD were positive for annexin V labeling but negative for propidium iodide staining. In addition, TCDD increased the area of the peak corresponding to hypodiploid (apoptotic) DNA content. All together these results support the hypothesis that TCDD toxicity in dPC12 cells takes place mainly through an apoptotic process. (C) 2010 Elsevier Inc. All rights reserved.”
“As the initial effort in a multi-step uncertainty analysis of a biologically based cancer model for formaldehyde, a Markov chain Monte Carlo (MCMC) analysis was performed for a compartmental model that predicts DNA-protein cross-links (DPX) produced by formaldehyde exposure. The Bayesian approach represented by the MCMC analysis integrates existing knowledge of the model parameters with observed, formaldehyde-DPX-specific data, providing a statistically sound basis for estimating model output uncertainty.